Imaging the Visual Network in the Migraine Spectrum

Abstract

The involvement of the visual network in migraine pathophysiology has been well-known for more than a century. Not only is the aura phenomenon linked to cortical alterations primarily localized in the visual cortex; but also migraine without aura has shown distinct dysfunction of visual processing in several studies in the past. Further, the study of photophobia, a hallmark migraine symptom, has allowed unraveling of distinct connections that link retinal pathways to the trigeminovascular system. Finally, visual snow, a recently recognized neurological disorder characterized by a continuous visual disturbance, is highly comorbid with migraine and possibly shares with it some common pathophysiological mechanisms. Here, we review the most relevant neuroimaging literature to date, considering studies that have either attempted to investigate the visual network or have indirectly shown visual processing dysfunctions in migraine. We do this by taking into account the broader spectrum of migrainous biology, thus analyzing migraine both with and without aura, focusing on light sensitivity as the most relevant visual symptom in migraine, and finally analyzing the visual snow syndrome. We also present possible hypotheses on the underlying pathophysiology of visual snow, for which very little is currently known.

Visual snow syndrome

“…The presence of associated visual symptoms, enhanced entoptic phenomena in particular, also potentially points to a disorder of habituation and sensory processing, which allows the perception of stimuli that are normally ignored by the brain. A migrainous pathophysiology alone, however, is not sufficient to explain the VS biology, primarily because of the chronic nature of this disorder as opposed to the ictal features of migraine, but also because most preventive migraine medication used empirically shows very little effect on VS. 23 An important issue with VS is the assumption that it could be due to HPPD. HPPD is a condition codified in DSM-V 24 and characterized by the re-experiencing of perceptual symptoms (flashbacks), typically of the visual type, that follow the cessation of the use of a hallucinogen and were experienced during the intoxication.…”

Occipital cortex and cerebellum gray matter changes in visual snow syndrome

“…Several pathophysiologic hypotheses for the genesis of VSS have been proposed in the literature, 27 and hyperexcitation of primary and secondary visual cortices 28 – 31 seems to be one of the most plausible. In a condition where internal visual information is constantly being perceived, a state of increased cortical activation, justified by a form of processing overload, is plausible.…”

Insular and occipital changes in visual snow syndrome: a BOLD fMRI and MRS study

“…5 VS pathophysiology is currently unknown; hypotheses include thalamo-cortical dysrhythmia of the visual pathways, 6 hyperexcitation of primary and secondary visual cortices, [7][8][9] increased saliency of normally ignored subcortical activity or perhaps a combination of all these mechanisms. 10 In particular, evidence for dysfunctional visual processing within the association cortices has emerged in VS, through the use of visual-evoked potentials. 7 An [ 18 F]-FDG PET study showed increased metabolism in the right lingual gyrus of VS patients compared to controls, implying a direct involvement of this area in VS pathophysiology.…”